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Inflammation in Atherosclerosis: Current Advances

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 December 2024 | Viewed by 662

Special Issue Editor


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Guest Editor
Research Institute of Internal Medicine, Oslo University Hospital, 0424 Oslo, Norway
Interests: atherosclerosis; cardiac involvement; Inflammation

Special Issue Information

Dear Colleagues,

Atherosclerosis is a chronic condition and is the main underlying cause of cardiovascular disease. The development and pathogenesis of atherosclerosis and its clinical consequences (e.g., myocardial infarction and ischemic stroke) are at the crossroads between metabolism and inflammation. Several current treatment therapies target the lowering of low-density lipoprotein cholesterol (LDL) levels. However, there are still a vast number of patients who experience cardiovascular complications. This residual risk is believed to be caused by persistent low-grade inflammation. In recent years, drugs targeting inflammation have been tested in randomized clinical trials with promising results. Pharmacological interventions targeting inflammation may provide new, better treatment outcomes and prevent future cardiac events. Still, there is a lack of knowledge of the molecular mechanisms of inflammation in atherosclerosis and how to target these pathways therapeutically.

This Special Issue will focus on future advancements in the mechanisms and regulation of inflammation in atherosclerosis.

Dr. Tuva B. Dahl
Guest Editor

Manuscript Submission Information

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Keywords

  • inflammation
  • atherosclerosis
  • cardiovascular disease

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Published Papers (1 paper)

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Research

17 pages, 5372 KiB  
Article
Quercetin Mitigates Lysophosphatidylcholine (LPC)-Induced Neutrophil Extracellular Traps (NETs) Formation through Inhibiting the P2X7R/P38MAPK/NOX2 Pathway
by Si Liu, Yan Wang, Linyao Ying, Hao Li, Keyi Zhang, Na Liang, Gang Luo and Lin Xiao
Int. J. Mol. Sci. 2024, 25(17), 9411; https://doi.org/10.3390/ijms25179411 - 30 Aug 2024
Viewed by 524
Abstract
Neutrophil extracellular traps (NETs) are three-dimensional reticular structures that release chromatin and cellular contents extracellularly upon neutrophil activation. As a novel effector mechanism of neutrophils, NETs possess the capacity to amplify localized inflammation and have been demonstrated to contribute to the exacerbation of [...] Read more.
Neutrophil extracellular traps (NETs) are three-dimensional reticular structures that release chromatin and cellular contents extracellularly upon neutrophil activation. As a novel effector mechanism of neutrophils, NETs possess the capacity to amplify localized inflammation and have been demonstrated to contribute to the exacerbation of various inflammatory diseases, including cardiovascular diseases and tumors. It is suggested that lysophosphatidylcholine (LPC), as the primary active component of oxidized low-density lipoprotein, represents a significant risk factor for various inflammatory diseases, such as cardiovascular diseases and neurodegenerative diseases. However, the specific mechanism of NETs formation induced by LPC remains unclear. Quercetin has garnered considerable attention due to its anti-inflammatory properties, serving as a prevalent flavonoid in daily diet. However, little is currently known about the underlying mechanisms by which quercetin inhibits NETs formation and alleviates associated diseases. In our study, we utilized LPC-treated primary rat neutrophils to establish an in vitro model of NETs formation, which was subsequently subjected to treatment with a combination of quercetin or relevant inhibitors/activators. Compared to the control group, the markers of NETs and the expression of P2X7R/P38MAPK/NOX2 pathway-associated proteins were significantly increased in cells treated with LPC alone. Quercetin intervention decreased the LPC-induced upregulation of the P2X7R/P38MAPK/NOX2 pathway and effectively reduced the expression of NETs markers. The results obtained using a P2X7R antagonist/activator and P38MAPK inhibitor/activator support these findings. In summary, quercetin reversed the upregulation of the LPC-induced P2X7R/P38MAPK/NOX2 pathway, further mitigating NETs formation. Our study investigated the potential mechanism of LPC-induced NETs formation, elucidated the inhibitory effect of quercetin on NETs formation, and offered new insights into the anti-inflammatory properties of quercetin. Full article
(This article belongs to the Special Issue Inflammation in Atherosclerosis: Current Advances)
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